Ventricular Tachycardia Torsade De Pointes Research Articles

Advanced integration of 2DCNN-GRU model for accurate identification of shockable life-threatening cardiac arrhythmias: a deep learning approach.

Cardiovascular diseases remain one of the main threats to human health, significantly affecting the quality and life expectancy. Effective and prompt recognition of these diseases is crucial. This research aims to develop an effective novel hybrid method for automatically detecting dangerous arrhythmias based on cardiac patients' short electrocardiogram (ECG) fragments. This study suggests using a continuous wavelet transform (CWT) to convert ECG signals into images (scalograms) and examining the task of categorizing short 2-s segments of ECG signals into four groups of dangerous arrhythmias that are shockable, including ventricular flutter (C1), ventricular fibrillation (C2), ventricular tachycardia torsade de pointes (C3), and high-rate ventricular tachycardia (C4). We propose developing a novel hybrid neural network with a deep learning architecture to classify dangerous arrhythmias. This work utilizes actual electrocardiogram (ECG) data obtained from the PhysioNet database, alongside artificially generated ECG data produced by the Synthetic Minority Over-sampling Technique (SMOTE) approach, to address the issue of imbalanced class distribution for obtaining an accuracy-trained model. Experimental results demonstrate that the proposed approach achieves high accuracy, sensitivity, specificity, precision, and an F1-score of 97.75%, 97.75%, 99.25%, 97.75%, and 97.75%, respectively, in classifying all the four shockable classes of arrhythmias and are superior to traditional methods. Our work possesses significant clinical value in real-life scenarios since it has the potential to significantly enhance the diagnosis and treatment of life-threatening arrhythmias in individuals with cardiac disease. Furthermore, our model also has demonstrated adaptability and generality for two other datasets.

Multifocal ectopic purkinje-related premature contractions and related cardiomyopathy.

In the past 20 years, genetic variants in SCN5A encoding the cardiac voltage-gated sodium channel Nav1.5 have been linked to a range of inherited cardiac arrhythmias: variants resulting in loss-of-function of Nav1.5 have been linked to sick sinus syndrome, atrial stand still, atrial fibrillation (AF) impaired pulse generation, progressive and non-progressive conduction defects, the Brugada Syndrome (BrS), and sudden cardiac death. SCN5A variants causing increased sodium current during the plateau phase of the cardiac action potential is associated with Long QT Syndrome type 3 (LQTS3), Torsade de Pointes ventricular tachycardia and SCD. Recently, gain-of-function variants have been linked to complex electrical phenotypes, such as the Multifocal Ectopic Purkinje-related Premature Contractions (MEPPC) syndrome. MEPPC is a rare condition characterized by a high burden of premature atrial contractions (PACs) and/or premature ventricular contractions (PVCs) often accompanied by dilated cardiomyopathy (DCM). MEPPC is inherited in an autosomal dominant fashion with an almost complete penetrance. The onset is often in childhood. The link between SCN5A variants, MEPPC and DCM is currently not well understood, but amino acid substitutions resulting in gain-of-function of Nav1.5 or introduction of gating pore currents potentially play an important role. DCM patients with a MEPPC phenotype respond relatively poorly to standard heart failure medical therapy and catheter ablation as the PVCs originate from all parts of the fascicular Purkinje fiber network. Class 1c sodium channel inhibitors, notably flecainide, have a remarkable positive effect on the ectopic burden and the associated cardiomyopathy. This highlights the importance of genetic screening of DCM patients to identify patients with SCN5A variants associated with MEPPC. Here we review the MEPPC phenotype, MEPPC-SCN5A associated variants, and pathogenesis as well as treatment options.

Arrhythmias related to antipsychotics and antidepressants: an analysis of the summaries of product characteristics of original products approved in Germany

PurposeMost psychiatric drugs, such as antidepressants (AD) and antipsychotics (AP), may cause cardiac adverse events (CAE). We used summaries of product characteristics (SmPC) for assessing the likelihood of AD and AP to cause CAE.MethodsWe identified all original medicinal products (OMP) of AD and AP approved in Germany. We searched for their SmPCs using the online services of PharmaNet.Bund, Gelbe liste®, Rote Liste®, Fachinfo-Service®, and via manufacturer contact. We extracted frequencies of reported CAE (QT prolongation, Torsade de Pointes tachycardia, and ventricular arrhythmia) and performed a risk assessment.ResultsWe obtained the SmPCs of 24 AD and 26 AP identified as OMP. Comparably high reported frequencies regarding QT prolongation were found for Invega® (paliperidone), Serdolect® (sertindole) (≥ 1/100 and < 1/10), and Zoloft® (sertraline) (≥ 1/10.000 and < 1/1000); regarding Torsade de Pointes tachycardia were found for Serdolect® (≥ 1/1000 to < 1/100), Zoloft®, and Trevilor® (venlafaxine) (≥ 1/10.000 and < 1/1000); regarding ventricular tachycardia for Solian® (amisulpride), Xomolix® (droperidol), Zyprexa® (olanzapine), and Trevilor® (≥ 1/10.000 and < 1/1000).ConclusionThe risk and frequency of CAE, as reported in the SmPCs, varied significantly among substances and between groups. There are more reports for AP than AD. The AP with the most frequently reported CAE (QT prolongation and Torsade de Pointes tachycardia) was Serdolect®; for AD, Zoloft® (QT prolongation, Torsade de Pointes tachycardia) and Trevilor® (Torsade de Pointes tachycardia and ventricular tachycardia) carried a higher cardiac risk.

Abstract 12650: A Faster and Safe Way for Dose Escalation of Sotalol Therapy in Patients With Atrial Fibrillation or Flutter

Sotalol is frequently employed to prevent the recurrence of highly symptomatic atrial fibrillation or flutter, but recurrence is not unusual and may require dose escalation. Sotalol can cause QTc prolongation proportional to blood concentration and at times may cause Torsade de Pointes ventricular tachycardia (TdP). Because the risk of TdP, dose escalation of oral sotalol therapy is mandated by FDA to be in-hospital for a minimum of 3 days under ECG monitoring with facilities and personnel able to provide cardiac resuscitation. With oral administration (bid), 3 days are needed to reach the new maximal steady-state blood concentrations (Cmax ss) and thus maximal QTc . Three hospital days in a telemetry bed is costly of time and resources. IV sotalol makes it possible to reduce the escalation time from 3 days to 1 day. The IV to oral dose escalation has been developed by model informed drug development. Serum sotalol concentrations and corresponding QTc were obtained from a bioequivalence study in healthy volunteers who received a single dose of oral and IV sotalol. NONMEM software package was used for population pharmacokinetic modeling and simulation. First Order Conditional Estimation method with Interaction (FOCE-INTER) was used for computation. We chose to administer IV sotalol over 1 hour to obtain the new Cmax ss target in a timeframe convenient for medical staff to supervise. Simulation for dose escalation from 80 to 120 mg bid is shown in the Figure; 75 mg IV sotalol is administered over 1 hour followed by 120 mg oral sotalol at 5 hours from start of infusion, then a second oral dose of 120 mg at 12 hours. One can target escalation from 120 to 160 mg by loading 90 mg IV over 1 hr followed by 160 mg oral dosing. Sotalol concentration will peak in 2-4 hours following each oral administration, thus in 21 hour there will be 3 sotalol peak concentrations. This permits evaluation of QTc response and risk of TdP all within a 1 day admission.

Abstract 12649: A Faster and Safe Way to Initiate Sotalol Therapy for Patients With Atrial Fibrillation or Flutter

Sotalol drug therapy is frequently employed to prevent the recurrence of highly symptomatic atrial fibrillation or flutter (AF, AFb). Sotalol can cause QTc prolongation that is proportional to blood concentration. Excessive concentration can cause Torsade de Pointes ventricular tachycardia (TdP). Because the risk of TdP, initiation of oral sotalol therapy is mandated by FDA to be in-hospital for a minimum of three days under ECG monitoring with facilities and personnel able to provide cardiac resuscitation. With oral administration (bid), 3 days are needed to reach maximal steady-state blood concentrations (Cmax ss) and thus maximal QTc prolongation. Three hospital days in a telemetry bed is costly and considerable expenditure of time and resources. Availability of IV sotalol makes it possible to reduce the loading time from 3 days to 1 day. The IV to oral loading regimen has been developed by model informed drug development. Serum sotalol concentrations and corresponding QTc were obtained from a previously performed bioequivalence study in healthy volunteers who received a single dose of oral and IV sotalol. NONMEM software package was used for population pharmacokinetic modeling and simulation. First Order Conditional Estimation method with Interaction (FOCE-INTER) was used for computation. We chose to administer IV sotalol over 1 hour to obtain Cmax ss target in a timeframe convenient for medical staff to supervise. The simulation for loading to the Cmax target produced by 80 mg PO bid is shown in the Figure; 60 mg IV sotalol is administered over 1 hour followed by 80 mg oral sotalol at 5 hours from start of infusion end then a second oral dose of 80 mg at 12 hours. One can target 120 mg maintenance dose by loading 90 mg IV over 1 hr followed by 120 mg oral dosing. Sotalol concentration will peak in 2-4 hours following each oral administration, thus in 21 hour there will be 3 sotalol peak concentrations. This permits evaluation of QTc response and risk of TdP all within a 1 day admission.

Drug use and torsades de pointes cardiac arrhythmias in Sweden: a nationwide register-based cohort study

ObjectiveTo study the occurrence of torsades de pointes (TdP) ventricular tachycardia in relation to use of drugs labelled with TdP risk, using two nationwide Swedish registers.DesignProspective register-based cohort study.SettingEntire Sweden.ParticipantsPersons...

RISK FACTORS ASSOCIATED WITH DOFETILIDE INTOLERANCE

Dofetilide is a class III antiarrhythmic requiring hospitalization for initiation due to the risk for torsades de pointes (TdP) ventricular tachycardia early in therapy. Dofetilide is subject to many drug interactions, which may increase the risk for intolerance. This is a single-center

Clinical pharmacists' opportunities to reduce inappropriate prescription of QT-prolonging medications: calls to action.

All biologically active agents carry the potential to lead to adverse reactions in certain individuals, including serious cardiac adverse reactions. Since 2005, there has been an international regulatory landscape governing the investigation of a new drug's propensity to lead to the polymorphic ventricular tachycardia Torsades de Pointes (Torsades), a rare but potentially fatal occurrence. When a regulatory agency considers it appropriate, warning information is placed in a medicine's patient information leaflet (label) concerning drug-induced QT interval prolongation, a phenomenon associated with Torsades. In busy hospital settings, however, prescribers, including cardiologists, make injudicious prescribing decisions that put patients at risk. The science of cardiac safety, including the clinical trials that generate the information about QT prolongation in patient information leaflets, is frequently not part of the curriculum at Schools of Pharmacy. Given that medication-induced cardiotoxicity is extremely serious, we advocate that schools integrate the science of cardiac safety into existing therapeutics/therapeutic medication monitoring courses. Given their expert knowledge of pharmacology, pharmacists working as part of a hospital's clinical team would then be even better placed to review prescribing decisions concerning medications that prolong the QT interval, and alert prescribers in cases where reassessing their decisions seems prudent. National pharmacy societies or other pertinent professional societies could create practice guidelines to support graduates once employed as clinical pharmacists. Clinical pharmacists are well placed to be influential arbiters of safer prescribing decisions. Cardiac safety education during their pharmacy training and practice guideline support from professional societies during their careers can optimize this role.

Congenital long QT syndrome in children

Long QT syndrome (LQTS) is a cardiac repolarization disorder characterized by prolonged QT interval on the electrocardiogram (ECG) and increased propensity to ventricular tachyarrhythmias and cardiac events. LQTS might be acquired or congenital, which presents a group of channelopathies that occur due to mutation in one of 15 so far identified genes. The most frequent types of congenital LTQS are LQT1, LQT2 and LQT3. Prolonged or delayed repolarization leads to the increase of action potential duration which predisposes early afterdepolarization, as well as the amplification of transmural dispersion of repolarization, both contributing to the development of Torsades de Pointes ventricular tachycardia. Clinical manifestations of LQTS are palpitations, syncope, aborted cardiac arrest or sudden cardiac death, but it can also be asymptomatic. Trigger factors for symptoms are specific for certain genotype. LQTS examination includes thorough clinical and family history focused on distinctive data (repeated syncopes, cases of sudden cardiac death in the family, hereditary arrhythmias), resting ECG, exercise stress testing and genetic analysis, with additional methods (serial ECG records, 24h ECG Holter, epinephrine test). Clinical LQTS diagnosis is based on Schwartz's scoring system, while the criteria for final diagnosis of LQTS depend on Schwartz's score, QT interval duration, presence of pathogenic mutation and clinical symptoms. Treatment approach begins with lifestyle modifications and β-blockers therapy, while other options include implantable cardioverter- defibrillator, permanent pacemaker or surgical sympathectomy. Sudden cardiac death is the reason of 90% of sudden deaths in young athletes, while LQTS is one of its causes. Recommendations for physical activities in children with congenital LQTS arise from the ones for adults and they presume very strict limitations. Further researches are expected to advance the understanding of genotype-phenotype correlation of congenital LQTS and enable eventual genetically-guided personalized treatment, novel insight into rare LQTS types, as well as more precise recommendations for physical activity of LQTS children.

The genetics underlying acquired long QT syndrome: impact for genetic screening.

Acquired long QT syndrome (aLQTS) exhibits QT prolongation and Torsades de Pointes ventricular tachycardia triggered by drugs, hypokalaemia, or bradycardia. Sometimes, QTc remains prolonged despite elimination of triggers, suggesting the presence of an underlying genetic substrate. In aLQTS subjects, we assessed the prevalence of mutations in major LQTS genes and their probability of being carriers of a disease-causing genetic variant based on clinical factors. We screened for the five major LQTS genes among 188 aLQTS probands (55 ± 20 years, 140 females) from Japan, France, and Italy. Based on control QTc (without triggers), subjects were designated 'true aLQTS' (QTc within normal limits) or 'unmasked cLQTS' (all others) and compared for QTc and genetics with 2379 members of 1010 genotyped congenital long QT syndrome (cLQTS) families. Cardiac symptoms were present in 86% of aLQTS subjects. Control QTc of aLQTS was 453 ± 39 ms, shorter than in cLQTS (478 ± 46 ms, P < 0.001) and longer than in non-carriers (406 ± 26 ms, P < 0.001). In 53 (28%) aLQTS subjects, 47 disease-causing mutations were identified. Compared with cLQTS, in 'true aLQTS', KCNQ1 mutations were much less frequent than KCNH2 (20% [95% CI 7-41%] vs. 64% [95% CI 43-82%], P < 0.01). A clinical score based on control QTc, age, and symptoms allowed identification of patients more likely to carry LQTS mutations. A third of aLQTS patients carry cLQTS mutations, those on KCNH2 being more common. The probability of being a carrier of cLQTS disease-causing mutations can be predicted by simple clinical parameters, thus allowing possibly cost-effective genetic testing leading to cascade screening for identification of additional at-risk family members.

Diclofenac Prolongs Repolarization in Ventricular Muscle with Impaired Repolarization Reserve

BackgroundThe aim of the present work was to characterize the electrophysiological effects of the non-steroidal anti-inflammatory drug diclofenac and to study the possible proarrhythmic potency of the drug in ventricular muscle.MethodsIon currents were recorded using voltage clamp technique in canine single ventricular cells and action potentials were obtained from canine ventricular preparations using microelectrodes. The proarrhythmic potency of the drug was investigated in an anaesthetized rabbit proarrhythmia model.ResultsAction potentials were slightly lengthened in ventricular muscle but were shortened in Purkinje fibers by diclofenac (20 µM). The maximum upstroke velocity was decreased in both preparations. Larger repolarization prolongation was observed when repolarization reserve was impaired by previous BaCl2 application. Diclofenac (3 mg/kg) did not prolong while dofetilide (25 µg/kg) significantly lengthened the QTc interval in anaesthetized rabbits. The addition of diclofenac following reduction of repolarization reserve by dofetilide further prolonged QTc. Diclofenac alone did not induce Torsades de Pointes ventricular tachycardia (TdP) while TdP incidence following dofetilide was 20%. However, the combination of diclofenac and dofetilide significantly increased TdP incidence (62%). In single ventricular cells diclofenac (30 µM) decreased the amplitude of rapid (IKr) and slow (IKs) delayed rectifier currents thereby attenuating repolarization reserve. L-type calcium current (ICa) was slightly diminished, but the transient outward (Ito) and inward rectifier (IK1) potassium currents were not influenced.ConclusionsDiclofenac at therapeutic concentrations and even at high dose does not prolong repolarization markedly and does not increase the risk of arrhythmia in normal heart. However, high dose diclofenac treatment may lengthen repolarization and enhance proarrhythmic risk in hearts with reduced repolarization reserve.

Fetal Long QT Syndrome Manifested as Atrioventricular Block and Ventricular Tachycardia: A Case Report and a Review of the Literature

Fetal onset of congenital long QT syndrome (LQTS) is a rare manifestation, and prenatal diagnosis is difficult. This report describes a boy who presented with both atrioventricular (AV) block and ventricular tachycardia during the antenatal period. The early postnatal electrocardiogram showed prolongation of the QT interval and AV block, subsequently leading to a polymorphic ventricular tachycardia torsade de pointes. This unique feature of congenital LQTS has a poor outcome, but the boy was successfully treated with beta-blockers and implantation of an automated cardioverter-defibrillator. The intrauterine manifestation of fetal AV block and ventricular tachycardia should raise a high suspicion of congenital LQTS, and the strong association with a malignant clinical course should warrant special evaluation. The literature on the prenatal diagnosis, fetal therapy, and neonatal outcome of this condition also are reviewed.

Assessing QT Interval Prolongation and its Associated Risks with Antipsychotics

Several antipsychotics are associated with the ventricular tachycardia torsade de pointes (TdP), which may lead to sudden cardiac death (SCD), because of their inhibition of the cardiac delayed potassium rectifier channel. This inhibition extends the repolarization process of the ventricles of the heart, illustrated as a prolongation of the QT interval on a surface ECG. SCD in individuals receiving antipsychotics has an incidence of approximately 15 cases per 10,000 years of drug exposure but the exact association with TdP remains unknown because the diagnosis of TdP is uncertain. Most patients manifesting antipsychotic-associated TdP and subsequently SCD have well established risk factors for SCD, i.e. older age, female gender, hypokalaemia and cardiovascular disease. QT interval prolongation is the most widely used surrogate marker for assessing the risk of TdP but it is considered somewhat imprecise, partly because QT interval changes are subject to measurement error. In particular, drug-induced T-wave changes (e.g. flattening of the T-wave) may complicate the measurement of the QT interval. Furthermore, the QT interval depends on the heart rate and a corrected QT (QTc) interval is often used to compensate for this. Several correction formulas have been suggested, with Bazett's formula the most widely used. However, Bazett's formula overcorrects at a heart rate above 80 beats per minute and, therefore, Fridericia's formula is considered more appropriate to use in these cases. Several other surrogate markers for TdP have been developed but none of them is clinically implemented yet and QT interval prolongation is still considered the most valid surrogate marker. Although automated QT interval determination may offer some assistance, QT interval determination is best performed by a cardiologist skilled in its measurement. A QT interval >500 ms markedly increases the risk for TdP and SCD, and should lead to discontinuation of the offending drug and, if present, correction of underlying electrolyte disturbances, particularly serum potassium and magnesium derangements. Before prescribing antipsychotics that may increase the QTc interval, the clinician should ask about family and personal history of SCD, presyncope, syncope and cardiac arrhythmias, and recommend cardiology consultation if history is positive.

Torsade de pointes, QT interval prolongation and renal disease

Torsade de pointes is a form of polymorphic ventricular tachycardia occurring in a setting of prolonged QT interval on surface electrocardiogram [1,2]. Several non-antiarrhythmic drugs [3–5] have been shown to prolong cardiac repolarization predisposing to torsade de pointes ventricular tachycardia. Blockade of the delayed rectifier (repolarising) potassium current and drug interactionswith inhibitors of the cytochromes P450 (CYP)-mediated metabolism are the most common underlying mechanisms [6,7]. Many antiarrhythmic drugs have been also implicated in prolonging QT interval and triggering torsades de pointes, especially during chronic therapy or in case of acute high dose toxicity [8]. Progressive renal disease is associated with an increased risk of cardiovascular death, specifically sudden death [9]. It has been reported that Corrected QT interval prolongation and torsade de pointes are associated with end-stage renal disease (ESRD) and that they can be a cause of sudden death in ESRD [10,11]. Moreover it has also been reported that left ventricular mass is increased from the earliest stages of renal disease (near normal renal function), the predominant pattern being eccentric left ventricular hypertrophy (LVH) and that LVH is linked to increased QT interval and dispersal, and with minor rhythm abnormalities, providing a link with the high risk of sudden death in this population too [9]. Furthermore electrolyte disturbances, bradycardia, female sex, advanced age, underlying heart disease have been reported as other risk factors predisposing to torsade de pointes [12–15]. We present a case of torsade de pointes in a 72-year-old Italian woman with chronic renal failure. A 72-year-old Italian woman was admitted to the Emergency Department. A history of chronic renal failure, a history of hypertension, a history of previous acute myocardial infarction and stroke were present. A history of recent hypotension was present too. Blood pressure values were 90/50 mm Hg, the oxygen saturation was 95% on room air. The patient was in treatment also with sotalol, with

Causes and Management of Drug-Induced Long Qt Syndrome

Long QT syndrome (LQTS) is characterized by inherited or acquired prolonged QT interval on the surface electrocardiogram. This can lead to torsade de pointes ventricular tachycardia (TdP VT) and ventricular fibrillation. In the acquired form of the disease, medications from several classes can cause TdP VT or potentiate the electrocardiographic findings. These include class IA and III antiarrhythmics, antibiotics (macrolides and quinolones), antidepressants (tricyclics and selective serotonin reuptake inhibitors), antipsychotics (haloperidol and phenothiazines), and antiemetics (ondansetron and prochlorperazine). We present four cases of drug-induced LQTS resulting in life-threatening cardiac arrhythmias. Antiarrhythmic medications were the cause in two cases, and the other two cases involved noncardiac medications. All four patients had at least one risk factor for LQTS in addition to the offending drug, including female gender, hypokalemia, hypomagnesemia, and bradycardia. In one patient, amiodarone was administered for treatment of VT, although the correct diagnosis was actually TdP VT. In patients with polymorphic VT or ventricular fibrillation without a significant history of cardiovascular disease, drug-induced LQTS should be high in the differential diagnosis. Prompt diagnosis is key, as amiodarone, while often used to suppress VT, is potentially harmful in the setting of LQTS and TdP VT.

Cardiotoxicity with 5‐fluorouracil and capecitabine: more than just vasospastic angina

In this case series we present a variety of different cardiac toxicities with 5-fluorouracil and its pro-drug capecitabine, including myocardial infarction, cardiomyopathy, sinoatrial and atrioventricular node dysfunction, takotsubo cardiomyopathy and QT prolongation with torsade-de pointes ventricular tachycardia. We stress the fact that while vasospasm is a well-recognized side-effect of this class of chemotherapeutic agent, broader cardiotoxicity is commonly seen and an increased awareness of the range of toxicity is necessary if repeat toxicity is to be avoided.

Survival after prolonged resuscitation with 99 defibrillations due to Torsade De Pointes cardiac electrical storm: a case report

A 48-year-old previously healthy woman suffered witnessed cardiac arrest in hospital. She achieved return of spontaneous circulation and was transferred to the intensive care unit. During the following 3 hours, she suffered a cardiac electrical storm with 98 episodes of Torsade de Pointes ventricular tachycardia rapidly degenerating to ventricular fibrillation. She was converted with a total of 99 defibrillations. There was no response to the use of any recommended anti arrhythmic drugs. However, the use of bretylium surprisingly stabilized her heart rhythm and facilitated placing of a temporary pacemaker. Overdrive pacing prevented further arrhythmias and was life saving. A number of beneficial factors may have contributed to the good neurological outcome. Further investigations gave no explanation for her cardiac electrical storm.

Life-threatening Torsades de Pointes resulting from “natural” cancer treatment

Introduction. Nonradioactive cesium chloride (CsCl) is used by some alternative medicine advocates as a treatment for cancer. The therapy was proven to be neither safe nor effective. Chronic use of CsCl has resulted in cases with severe cardiotoxicity. Case report. A 65-year-old lady presented to our hospital's accident and emergency department with recurrent syncope attacks. Electrocardiogram monitoring showed QT prolongation and transient Torsades de Pointes (TDP) ventricular tachycardia. She was taking anticancer naturopathic drugs for 6 weeks before admission. One of her naturopathic drugs was subsequently confirmed containing 89% CsCl by weight. Besides conventional treatment of QT prolongation and TDP, the patient was given a 4-week course of oral Prussian blue to enhance gastrointestinal elimination of cesium. The serum half-life of cesium was reduced from 61.7 to 29.4 days after the use of Prussian blue. QT prolongation was normalized in 27 days. Discussion. To our knowledge, this is the first published case of nonradioactive cesium poisoning treated with Prussian blue. A transient rise in serum cesium level was observed during Prussian blue therapy. Possible explanations for this observation include poor drug compliance during outpatient treatment and redistribution of cesium from body stores. Conclusion. Nonradioactive CsCl poisoning can result in severe cardiotoxicity with QT prolongation and TDP ventricular tachycardia. The key points in the management of nonradioactive cesium poisoning include cessation of cesium exposure, vigorous electrolytes replacement, and oral Prussian blue therapy.

Abstract 2642: Prevalence and Importance of Cardiac Arrhythmias after Acute Ischemic Stroke

Although heart rhythm monitoring following acute ischemic stroke is widely practiced, the prevalence of arrhythmia during the acute phase of ischemic stroke is debated. Several studies have claimed the potential threat of QT prolongation possibly leading to Torsades de Pointes ventricular tachycardia (VT) or ventricular fibrillation (VF). Furthermore, knowledge of the true rate of occult atrial fibrillation (AF) among ischemic stroke patients is sparse. 224 consecutive patients with acute ischemic stroke underwent daily 12-lead ECG during the first 5 days after hospital admission; as well as 24 hour Holter monitoring was performed in all patients. Patients with prior AF, established ischemic heart disease and heart failure were excluded. Patients were followed for 40 months for vital status. The mean age of the patients was 69 years. No patient had VT or VF. Previously unsuspected AF could be demonstrated in only 13 of 224 patients (6%). All 13 were detected by Holter monitoring, while nearly half were missed by ECG. During follow-up 53 (24 %) patients died. The presence of AF was significantly associated with mortality (log-rank p &lt;0.0001; Figure ). In Cox analysis, patients with AF had an increased mortality compared to patients without AF (HR=2.44; [95 % CI, 1.00 – 6.00], P = 0.05) with adjustment for age and stroke severity and renal failure. The fear of serious ventricular arrhythmias in the acute phase of ischemic stroke appears to be groundless. However, new onset AF can be demonstrated in one of 20 patients with acute ischemic stroke and seems to be associated with an increased mortality during long-term follow-up.

Successful Conversion of Recent‐onset Atrial Fibrillation by Sequential Administration of up to Three Antiarrhythmic Drugs

Short-term conversion attempt of recent-onset atrial fibrillation (AF) in the emergency room fails too often. Many patients and doctors still prefer pharmacological to electrical solutions in such cases. Sequential administration of up to 3 antiarrhythmic drugs of different classes of action (amiodarone, propafenone, and quinidine) may achieve conversion in such patients. One hundred and forty consecutive patients with recent-onset AF were transferred to the intensive cardiac care unit after a failed 2-h conversion attempt in the emergency room. First-line drug for conversion was continued up to a full dose, and was chosen by AF etiology, or in recurrent AF episodes, empirically. In nonresponders, the failed drug was replaced by a drug of another class, and if the second-line drug failed it was replaced by a drug of the third-line. Electrical cardioversion was the final solution for nonresponders. Sixty percent of patients reached sinus rhythm by the first-line drug therapy, 34% by the second-line, and 4% by the third-line. Seventy-five percent of patients achieved conversion within 26 h, and 95% of patients achieved conversion within 40 h. Three patients were electrically cardioverted due to hemodynamical instability. Two episodes of Torsade de Pointes ventricular tachycardia were self-terminated. Sequential usage of up to 3 antiarrhythmic drugs of different classes of action provides almost complete success in conversion of recent-onset AF in patients refractory to short-term conversion attempt in the emergency room.